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Nicotine has long been characterized as having two phases of action on the heart, initially negative and subsequently positive chronotropic and inotropic effects. The nicotine-induced inhibition has been generally assumed to be due to activation of the nicotinic receptors on the cardiac ganglion cells that fires the axons, liber ates acetylcholine (ACh) and eventually inhibits atrial contractions (Giotti, 1954; Leaders and Long, 1962; Chiang and Leaders, 1965; Khan et al. 1965; Long and Gross, 1966; Chiang and Leaders, 1968). Odawara and Nishi (1980) have shown, however, that the nicotine-induced inhibition of the isolated guinea-pig atrium can occur after blockade of the nerve conduction by tetrodotoxin. They reported that the axon terminals of cardiac ganglion cells are endowed with nicotinic recep-

Propranolol blocks the extrasynaptic nicotinic receptors on the intramural cardiac ganglion cells.